Resistance to oncogenic transformation in revertant R1 of human ras-transformed NIH 3T3 cells

Journal Article · Mon May 01 00:00:00 EDT 1989 · Mol. Cell. Biol.; (United States)

DOI:https://doi.org/10.1128/MCB.9.5.2258· OSTI ID:5703338

Kuzumaki, N; Ogiso, Y; Oda, A; Fujita, H; Suzuki, H; Sato, C; Mullauer, L

A flat revertant, R1, was isolated from human activated c-Ha-ras-1 (hu-ac-Ha-ras) gene-transformed NIH 3T3 cells (EJ-NIH 3T3) treated with mutagens. R1 contained unchanged transfected hu-ac-Ha-ras DNA and expressed high levels of hu-ac-Ha-ras-specific mRNA and p21 protein. Transfection experiments revealed that NIH 3T3 cells could be transformed by DNA from R1 cells but R1 cells could not be retransformed by Kirsten sarcoma virus, DNA from EJ-NIH 3T3 cells, hu-ac-Ha-ras, v-src, v-mos, simian virus 40 large T antigen, or polyomavirus middle T antigen. Somatic cell hybridization studies showed that R1 was not retransformed by fusion with NIH 3T3 cells and suppressed anchorage independence of EJ-NIH 3T3 and hu-ac-Ha-ras gene-transformed rat W31 cells in soft agar. These results suggest that the reversion and resistance to several oncogenes in R1 is due n not to cellular defects in the production of the transformed phenotype but rather to enhancement of cellular mechanisms that suppress oncogenic transformation.

• Research Organization: Hokkaido Univ., Sapporo (Japan). School of Medicine
• OSTI ID: 5703338
• Journal Information: Mol. Cell. Biol.; (United States), Vol. 9:5
• Country of Publication: United States
• Language: English

Related Subjects

59 BASIC BIOLOGICAL SCIENCES
GENE REPRESSORS
GENE AMPLIFICATION
ONCOGENES
MOLECULAR BIOLOGY
ONCOGENIC TRANSFORMATIONS
GENE REGULATION
SOMATIC CELLS
HYBRIDIZATION
GENETIC ENGINEERING
HUMAN POPULATIONS
MESSENGER-RNA
MUTAGENS
ONCOGENIC VIRUSES
SENSITIVITY
ANIMAL CELLS
CELL TRANSFORMATIONS
GENES
MICROORGANISMS
NUCLEIC ACIDS
NUCLEOPROTEINS
ORGANIC COMPOUNDS
PARASITES
POPULATIONS
PROTEINS
RNA
VIRUSES
550200* - Biochemistry
550400 - Genetics